Khalili H, Deshpande R, Chang M Y
Department of Medicine, North Shore University Hospital, New York University Medical College, Manhasset 11030, USA.
Immunology. 1997 Dec;92(4):487-93. doi: 10.1046/j.1365-2567.1997.00369.x.
We have previously reported that placental macrophages of fetal origin have a decreased ability to present antigen. To clarify the underlying mechanism for this deficiency, we have generated primary fetal macrophage cell lines. Our data show that despite their defective antigen-presenting ability, fetal macrophages do express all known accessory molecules, intracellular adhesion molecule-1, B7 and major histocompatibility complex class II molecules. However, fetal macrophages do not express detectable invariant chain mRNA which is known to have a major role in the class II-associated antigen-processing pathway. Since fetal macrophages can neither present antigenic peptides nor superantigen, the diminished invariant chain expression alone cannot account for the impaired antigen-presenting function of fetal macrophages.
我们之前曾报道，源自胎儿的胎盘巨噬细胞呈递抗原的能力有所下降。为阐明这种缺陷的潜在机制，我们建立了原代胎儿巨噬细胞系。我们的数据表明，尽管胎儿巨噬细胞的抗原呈递能力存在缺陷，但它们确实表达所有已知的辅助分子、细胞间黏附分子-1、B7以及主要组织相容性复合体II类分子。然而，胎儿巨噬细胞不表达可检测到的恒定链mRNA，而恒定链在II类相关抗原加工途径中起主要作用。由于胎儿巨噬细胞既不能呈递抗原肽也不能呈递超抗原，仅恒定链表达的减少并不能解释胎儿巨噬细胞抗原呈递功能受损的原因。
